Evidence Hub

Effect of LTRA on IP-10-induced eosinophil adhesion to ICAM-1

Toru Noguchi, K. Nakagome, Takehito Kobayashi, Yutaka Ueda, Yoshitaka Uchida, Tomoyuki Soma, H. Nakamoto, M. Nagata

Allergology International, 2016

6 citations

Abstract

Cysteinyl leukotrienes (cysLTs), such as LTC4, LTD4, and LTE4, can augment the accumulation of eosinophils in the tissues of asthmatic airways. We previously reported that LTD4 up-regulates the expression of b2 integrins on human eosinophils in vitro and increases eosinophil adhesion.1 We also reported that LTD4 directly induces transendothelial migration, superoxide anion generation, and the degranulation of eosinophils.2 Administration of leukotriene receptor antagonist (LTRA) reduces the number of eosinophils in sputum of asthmatics, which supports the role of cysLTs in the accumulation of eosinophils in airways. Moreover, recent evidence suggests that cysLTs are increased in the airways during virus-induced asthma.3 As the numbers of eosinophils and neutrophils increase in asthmatic airways during virus infection, cysLTs may be involved in the virus-induced enhancement of eosinophilic inflammation. Therefore, LTRA may provide a useful strategy for controlling virus-induced eosinophilic airway inflammation and asthma exacerbation. Interferon-g-inducible protein of 10 kDa (IP-10) is involved in the virus-induced exacerbation of asthma. For example, rhinovirus (RV) infection induces bronchial epithelial cells to produce IP-10 in vitro and in vivo, and serum IP-10 concentrations are specifically increased in RV-induced asthma exacerbation.4 The increased levels of IP-10 correlate with disease severity during RV-induced exacerbation. IP-10 binds to CXCR3 expressed on…

Read the paper

Related studies

Go deeper in Evidence Hub

Evidence Hub adds a study data sheet (design, sample size, evidence level, key numbers), an AI summary and a chat grounded in the paper's text.

Open this study Sign up free